Flashcards in introduction to the immune system Deck (26)
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1
What is Immunology?
Immunology is the study of our body's sytems for preventing and treating diseases.
2
How is the Immune System organized?
Innate Immunity - and a second, more specific defence -
Adaptive Immunity. The adaptive immunity can be humoural (ie. B cells and antibodies) or it can be cellular (ie. T cells). White Blood Cells (WBCs) are key players in the immune system.
3
what are the components of innate immunity?
βphysical barriers ( skin, mucosal surfaces)
βchemical barriers ( pH, secreted factors)
βphagocytes (monocytes/granulocytes/neutrophils)
βinflammation
β acute phase response
βcytokines and chemokines
βcomplement
βnatural killer cells
4
what is the inflammatory response triggered by?
β the release of pro-inflammatory cytokines and chemokines at the site of infection
5
what is the purpose of the inflammatory response?
βlocalize and eliminate injurious agents and to remove damages tissue components
6
what occurs during the inflammatory response?
βenhanced permeability and extravasation
βneutrophil recruitment
βenhanced cell adhesion
β enhanced clotting
7
what are cytokines and chemokines?
glycoprotein hormones that affect the immune response
8
what do cytokines do?
they act to modify the behavior of cells in the immune response
most of them are called interleukins
9
what do chemokines do?
act as chemotactic factors that create concentration gradients which attract or repel certain cell types to a site of infection or production
10
how do macrophages detect microbes?
βMacrophages have phagocytic receptors that bind microbes and their components.
βThey detect substances that are usually presented on pathogens (non-self).
11
what are protein-associated molecular patterns PAMPs and give some examples?
βPAMPs are small molecular motifs conserved within a class of microbes.
β glycans
β lipopolysaccharides
βbacterial flagellin
β lipoteichoic acid
β peptidoglycan
βnucleic variants normally associated with viruses, such as double-stranded RNA
12
what are damage-associated molecular patterns (DAMPs) and give some examples
βDAMPs are molecules released by stressed cells undergoing necrosis.
βvary greatly depending on the type of cell and injured tissue.
βSome of these endogenous danger signals are proteins
β heat-shock proteins and cytokines.
βNon-protein DAMPs include ATP, heparin sulfate and DNA.
13
what are pattern recognition receptors? (PRR) and what are they encoded by?
βhost factors that specifically recognize a particular type of PAMP.
β germ-line encoded.
14
what are the three types of PRR?
EXTRACELLULAR:
βthey recognize PAMPs outside of a cell and trigger a coordinated response to the pathogen
INTRACELLULAR (CYTOPLASMIC):
βrecognize PAMPs inside a cell and act to coordinate a response to the pathogen
SECRETED:
βact to tag circulation pathogens for elimination
15
how does interferon work?
βA virus infects a cell, which then becomes known as the primary infected cell.
β virus will multiply inside the cell, and, after the cell dies, it will release the viral progeny.
βas the primary infected cell is dying, it releases interferons.
βinterferons are picked up by other healthy cells, and they induce the transcription of >400 antiviral genes.
β healthy cells in an antiviral state so viruses cannot affect them.
16
what is the ligand and outcome of lectin receptors?
LIGAND: terminal mannose, fucose
OUTCOME: phagocytosis
17
what is the ligand and outcome of scavenger receptors?
LIGAND: bacterial cell walls, modified low-density lipoproteins
OUTCOME: phagocytosis
18
what is the ligand and outcome of Toll like receptors?
LIGAND: lipopolysaccharides together with CD14 (LPS), lipoproteins, unmethylated CpG, flagellin, dsRNA and ssRNA (in endosomes)
OUTCOME: phagocytosis, inflammation,
19
what is the ligand and outcome of NOD like receptors?
LIGAND: peptidoglycan from Gram-positive and negative bacteria, some viral DNA and
RNA
OUTCOME: inflammation, cytokine release (IL-1, IL-8)
20
what is the ligand and outcome of RIG-like receptors?
LIGAND: dsRNA and 5'-triphosphate RNA
OUTCOME: type I interferon production
21
what are complement proteins?
βA system of secreted proteins made in the liver that recognise PAMPs on the surface of microbes and 'decorate' or 'tag' them.
βThe microbes are then cleared by phagocytosis, "opsonised" (C3 sticks to pathogen membranes) or they have holes punched in them.
22
what are the three pathways of activating complement proteins?
βrecognition of LPS and other PAMPs by the C1q component of the 'classical' pathway
β non-host glycosylation is recognised by MBP (mannan/mannose-binding protein) and other lectins to activate the 'lectin' pathway
β membranes that are recognised as "non-self" activate the 'alternative' pathway Complement activation involves a proteolytic cascade.
23
what is the structure of natural killer cells?
βthey are large granular lymphocytes.
βthey make up about 4% of WBCs.
β lymphocyte-like, but larger with a granular cytoplasm.
β kill certain tumour cells and virally-infected cells.
β Target cell destruction is caused by the cytotoxic molecules called granzymes and perforins.
24
how are natural killer cells activated?
βNatural killer (NK) cells are activated by loss-of-self.
βAn NK cell has an MHC receptor on its surface.
βWith an uninfected cell, it will present the ligand for the MHC receptor, stimulating an inhibitory signal that stops the NK cell from killing it.
β with an infected cell, they do not present this ligand, so the inhibitory signal is not presented
βreleases perforin and cytotoxic granules into the infected cell or engages the cell's death receptors.
25
there are specific diseases associated with innate immunity what are they?
βcomplement
β core defects (eg. C3) linked to the development of autoimmune diseases such as lupus
complement
β non-core defects linked to susceptibility to specific types of pathogens such as Neisseria (meningitis)
macrophage deficiencies
β chronic granulomatous disease (CGD); no oxidative burst for bacterial killing
macrophage deficiencies
β IRF8 (transcription factor) mutations linked to susceptibility to TB
β Aicardi-Goutieres syndrome is associated with constitutive production of inflammatory cytokines (defect in regulation of cytokines)
β lack of interferon-responsiveness
β sensitivity to viral infections (eg. measles)
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